Release of cysteinyl leukotrienes with aspirin stimulation and the effect of prostaglandin E-2 on this release from peripheral blood leucocytes in aspirin-induced asthmatic patients
G. Celik et al., Release of cysteinyl leukotrienes with aspirin stimulation and the effect of prostaglandin E-2 on this release from peripheral blood leucocytes in aspirin-induced asthmatic patients, CLIN EXP AL, 31(10), 2001, pp. 1615-1622
Background The decrease in prostaglandin E-2 (PGE(2)) release due to aspiri
n (ASA)induced cyclooxygenase inhibition and the increment in cysteinyl leu
kotriene (Cys-LT) release secondary to the removal of the inhibitory effect
of PGE(2) on Cys-LT release have been suggested in the pathogenesis of asp
irin-induced asthma (AIA).
Objective In this study, we aimed to investigate the in vitro release of Cy
s-LT and to determine the effect of PGE(2) on Cys-LT release from periphera
l blood leucocytes of patients with AIA after stimulation by ASA.
Patients and methods Patients with AIA (n = 13), patients with ASA-tolerant
asthma (ATA) (n = 12) and healthy volunteers as controls (n = 13) were inc
luded to the study. ASA and PGE(2) at three different concentrations were a
pplied to the peripheral blood leucocytes of the study group, and Cys-LT le
vels following stimulants were assessed by enzyme immunoassay method.
Results There was no difference in baseline Cys-LT levels between groups (A
IA 353.4 +/- 55.5 pg/mL, ATA 354.7 +/- 40.3 pg/mL, and control group 368.5
+/- 30.2 pg/mL; P > 0.05). Though not present in other groups, the Cys-LT l
evel of 453.6 +/- 70.0 pg/mL following ASA stimulation was higher than base
line in patients with AIA (P = 0.04). When PGE2 was added to the ASA-stimul
ated samples of patients with AIA, Cys-LT levels were measured as 298.7 +/-
78.6 pg/mL, 279.8 +/- 79.9 pg/mL, and 243.4 +/- 51.3 pg/mL at PGE(2) 10(-7
) M, 10(-6) M and 10(-5) M concentrations, respectively. These levels were
lower than the ASA-stimulated Cys-LT values (P = 0.03, P = 0.01 and P = 0.0
1, respectively). The inhibitory effect of different PGE(2) concentrations
on Cys-LT release was also present in patients with ATA and in controls.
Conclusion The increase in Cys-LT levels following ASA stimulation seems to
be unique to AIA, which was not present in patients with ATA and in health
y controls. The inhibitory effect of PGE(2) on stimulated Cys-LT levels is
another important finding to elucidate the role of PGE(2) in the pathogenes
is of AIA.